Journal of Electromyography and Kinesiology 15 (2005) 240255

www.elsevier.com/locate/jelekin

Electrophysiology and kinesiology for health and disease

Toshio Moritani *, Tetsuya Kimura, Taku Hamada, Narumi Nagai
Laboratory of Applied Physiology, Graduate School of Human and Environmental Studies, Kyoto University, Kyoto 606-8501, Japan

Abstract
This paper summarizes my Basmajian keynote presentation at the 2004 International Society of Electrophysiology and Kinesiology Conference. I dedicate this paper to Dr. Herbert A. deVries, the mentor of my research career. The following topics will be
covered from the standpoint of Electrophysiology and Kinesiology for health and disease: (1) electromechanical manifestations of
neuromuscular fatigue and muscle soreness, (2) cardiac depolarizationrepolarization characteristics of normal and patients, (3) etiology of obesity and diabetes and autonomic nervous system, and (4) functional electrical stimulation for health and disease,
respectively.
2005 Elsevier Ltd. All rights reserved.

1. Electromechanical manifestations of neuromuscular

fatigue and muscle soreness
1.1. Delayed onset of muscle soreness
Every sports participant would experience muscle
soreness after training. A typical feature of muscle soreness is its delayed onset, and therefore this type of muscle soreness is usually called delayed onset of muscle
soreness (DOMS) [27]. It is the sensation of discomfort
or pain in the skeletal muscles that occur following
unaccustomed eccentric exercise [3]. It can usually be felt
within 8 or 10 h after exercise, peaks between 24 and 48
h and it is gone in about 57 days post-exercise. Sore
muscle can be described as being sti or tender because
there is a sense of reduced mobility or exibility, and the
muscles are sensitive, particularly upon palpation or
movement, sometimes feeling swollen [47]. The most
commonly raised possibly cause of DOMS are: (i) damage to the muscle bers themselves, connective tissue, (ii)
edema, inammation and swelling, and (iii) a vicious cycle of reex muscle activity, ischemia and painspasm
*

Corresponding author. Tel./fax: + 81 75 753 6888.

E-mail address: moritani@virgo.jinkan.kyoto-u.ac.jp (T. Moritani).

1050-6411/$ - see front matter 2005 Elsevier Ltd. All rights reserved.
doi:10.1016/j.jelekin.2005.01.001

theory. Although a number of dierent mechanisms

were proposed in the past, the exact nature of this
DOMS and its association to the spinal alpha motoneuron excitability and blood circulation has not yet clearly
been established.
We investigated the physiological eects of static
stretching upon DOMS in conjunction with the spinal
alpha motoneuron pool excitability and peripheral muscle blood ow in seven healthy male subjects. All subjects performed heel raises (30 rep, 5 sets) with 20 kg
load 24 h prior to testing. Electrophysiological measurements included the Homan reex amplitude (H amplitude) as a measure of spinal alpha motoneuron pool
excitability. The directly evoked muscle action potential
(M-wave) remained constant for each subject throughout the experiments. The posterior tibia nerve was electrically stimulated for this purpose [38]. Blood ow was
performed by near infrared spectroscopy (NRS). In the
experimental condition (EXP), those measurements
were obtained before/after static stretching (35 s, 3 sets)
under experimentally induced muscle soreness. During
the control condition (CON), the same measurements
were made before/after standing rest for a period of 4
min. The order of the experimental treatments (EXP
or CON) were chosen at random.

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Fig. 1 represents a typical set of H-reex data obtained 24 h after experimentally induced muscle soreness
prior to muscle stretching and immediately after muscle
stretching. The data clearly indicated that H-reex
amplitude was considerably reduced after muscle
stretching. Group data demonstrated that the static
stretching brought about a statistically signicant reduction in the H/M ratio (23.5%, p < 0.01) of the EXP conditions while no such changes were observed in CON
trials. These changes were accompanied by nearly
78.5% increase (p < 0.01) in blood ow after stretching
of the leg with the experimentally induced soreness.
The result of reduction in alpha motoneuron excitability
was entirely consistent with earlier studies, suggesting
that the inverse myotatic reex (Ib inhibition) may be
the basis for the relief of muscle soreness by static
stretching. The increase in blood ow after stretching
found in the present study suggested that static stretching could bring about a relief of spasm, which could
have caused local muscles ischemia and pain. Our data
strongly suggest that static stretching plays a signicant
role in relief of DOMS by reducing spinal motoneuron
pool excitability and enhancing muscle blood ow (see
Fig. 2).
1.2. Fusimotor sensitivity after prolonged stretch
shortening cycle exercise
We have recently performed comparative analyses of
T-reex, elicited by Achilles tendon tap and H-reex,
elicited by electrical stimulation of tibial nerve before
and immediately after, 2- and 24-h after two hours of
exhaustive running (n = 10). Results revealed that immediately after the running T and H wave amplitudes were
signicantly depressed while maximal M-wave remained
constant. On the other hand, 2-h after the running H-

241

reex amplitudes showed clear-cut rising (p < 0.001)

and by contrast, the T-reex amplitude did not show
such a signicant elevation. All the EMG amplitudes
recovered to the preexercise level in 24 h. The impact
force on the Achilles tendon (coecient of rebound
force) showed a reduction immediately after the running
(p < 0.05) and recovered in 24 h. The dierence between
H- and T-reex amplitudes 2-h after the exhaustive running might suggest that the sensitivity of fusimotor
activity was reduced by 2-h of running. Furthermore
the reduced impact force might signify deteriorated stiness regulation of muscle-tendon complex. This may
also suggest the degradation of spindle activity. Therefore, present results support the hypothesis claiming that
the stretch reex reduction might be attributed to disfacilitation of alpha motoneuron pool caused by withdrawal of spindle-mediated fusimotor support and/or
fatigue of the intrafusal bers of muscle spindle itself
[4,5].
1.3. Use of mechanomyogram for analysis of motor unit
activity
Previous studies have indicated that mechanomyogram (MMG) amplitude and frequency components
might represent the underlying motor unit (MU) recruitment and ring rate (rate coding) [6,4952]. Interestingly, MMG amplitude actually decreases at higher
force levels at which MUs might be ring at tetanic
rates, causing a fusion-like contraction leading to diminished MMG amplitude, while its frequency increases
[41,73,74]. These data suggest that MMG analyses
might oer not only MU recruitment and rate coding
characteristics, but also their mechanical properties,
i.e., the fusion properties of activated MUs that could
not be obtained by conventional EMG analyses [41,74].

Fig. 1. Spinal motoneuron excitability (H-reex) changes following experimentally-induced muscle soreness (a) and after static muscle stretching (b).

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Fig. 2. A simplied schematic representation of basic neural components involved in stretch reex and Golgi tendon organ Ib inhibition.

To further shed some light on this matter, we studied

14 isolated MUs in the medial gastrocnemius (MG) muscle of 7 healthy male subjects. Two identical microphone
sensors (10 mm diameter, mass 5 g, bandwidth 32000
Hz) for MMG recording were xed to the center of the
belly of the MG and soleus (SOL). Single twitch and
repetitive stimulations (10 Hz) were performed during
room temperature and hypothermic conditions (15, 20,
and 25 C) [26]. During voluntary contractions,
MU and MMG activities were recorded at 20%, 40%,
60%, and 80% MVC. Eects of mixed micro-stimulations
were also studied by stimulating two MUs at 510, 10
20, 812, and 1224 Hz, respectively; while simultaneously recorded evoked mass action potentials
(M-wave) remained constant. In addition, isolated MU
fatigue trials were performed at 12 Hz for a period of
2-min in order to determine the relationship between
muscle contractile slowing and the corresponding
MMG amplitude and frequency components (see Fig. 3).
The group data indicated that rms-MMG of MG increased as a function of force (p < 0.01). On the contrary, these values for SOL increased up to 60% MVC
(p < 0.01), but then decreased at 80% MVC due to possible MU fusion resulting in smaller muscle dimensional
changes [41,73]. Similarly, a signicant reduction in the
muscle contractile properties (peak force, maximal rate
of force development and relaxation, contraction and
half-relaxation times, etc.) caused by the experimental
hypothermia also resulted in signicant reduction in
MMG amplitude with subsequent fusion at a low stimulation frequency [26]. Dierent stimulation frequency
trials indicated that there were highly signicant and
progressive reductions in the force uctuations from 5
to 50 Hz that were almost mirrored by the similar and

signicant reductions in the MMG amplitudes. Mixed

stimulations to dierent MUs clearly demonstrated that
both MMG and force recordings showed two distinguished peak frequencies that were delivered to the
underlying MUs. Lastly, our MU fatigue study with
prolonged stimulation at 12 Hz demonstrated that
MMG amplitude decreased progressively as contractile
slowing occurred as a function of time (see Fig. 4).
1.4. Mechanomyogram changes during low back muscle
fatigue
As a practical application of this MMG analysis, we
have recently investigated the etiology of low back muscle fatigue by means of simultaneous recordings of
EMG, MMG, and near infrared spectroscopy (NIRS)
in an attempt to shed some light on the electrophysiologic, mechanical, and metabolic characteristics, respectively [75]. Eight male subjects performed back
extension isometrically at an angle 15 with reference
to the horizontal plane for a period of 60s. Surface
EMG, MMG and NIRS signals were recorded simultaneously from the center of the belly of L3. NIRS were
measured to determine the level of muscle blood volume
(BV) and oxygenation (Oxy-Hb). The root mean square
amplitude value (rms) of EMG signicantly increased at
the initial phase of contraction and then fell signicantly
while mean power frequency (MPF) of EMG was significantly and progressively decreased as a function of
time. There were also signicant initial increases in
rms-MMG, which was followed by progressive
decreases at the end of fatiguing contractions. MPFMMG remained unchanged. BV and Oxy-Hb dramatically decreased at the onset of the contraction and then

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243

Fig. 3. Mechanomyogram changes obtained from isolated motor unit during direct stimulation at dierent frequencies.

remained almost constant throughout the rest of contraction. These results obtained by simultaneous recordings of EMG, MMG, and NIRS tools demonstrates that
restriction of blood ow due to the high intramuscular
mechanical pressure is one of the most important factors
to evoke the muscle fatigue particularly in low back
muscle. In addition, our simultaneous recording system
described here can obtain more reliable information
regarding the mechanism(s) of low back muscle fatigue.

2. Cardiac depolarizationrepolarization characteristics

of normal and patients with long QT syndrome (LQTS)
Cardiac autonomic dysfunction is prevalent in cardiac and diabetic patients and associated with prolongation of the myocardial repolarization period. It has been
speculated that changes in autonomic nervous system
activity, particularly the sympatho-vagal balance contributes to the prolongation of myocardial repolarization. Therefore, a prolonged heart rate-adjusted ECG
QT duration (QTc) has been used as a marker for sudden cardiac death in myocardial infarction patients
[61,62]. There is also increasing evidence that a prolonged QTc is predictive of coronary heart disease mor-

tality in healthy populations as well [60]. Although the

importance of the QTc interval is clearly recognized, it
is often dicult to determine the end of the T(U) wave
and to measure the QT interval precisely because of a
variety of morphological T(U) wave abnormalities such
as biphasic, or notched T-waves in patients [60]. In the
latent or borderline patients, exercise stress testing, isoproterenol infusion, or autonomic maneuvers such as
the Valsalva maneuver or the cold pressure test are reported to be helpful in unmasking a prolonged QT interval. However these provocative maneuvers are stressful
and may occasionally be dangerous in some LQTS
patients.
Therefore, attempts to identify new quantitative ECG
characteristics of LQTS using a computer algoritlm have
recently been made [7,21]. For example, the activation
recovery interval (ARI), dened as the interval between
the minimum dV/dt of the QRS and the maximum dV/dt
in the STT segment on ECG, has been proposed as a
useful measure of local repolarization duration. Likewise, transmembrane activation time (AT) has been reported to occur at the intrinsic deection, the interval
between ECG QRS onset to the time of maximal dV/
dt of the T waves. More recent studies including our
own work [67,70] have estimated the myocardial depolarizationrepolarization process in terms of recovery

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Fig. 4. Mechanomyogram changes obtained from isolated motor unit during 12 Hz prolonged fatigue stimulation.

time (RT) dened as the total time of AT and ARI and

assessed quantitatively the degree of myocardial ischemia instead of evaluating changes in ST-segment and
QT interval (see Fig. 5).
2.1. Cardiac recovery time of normal and patients
It has been suggested that QTc prolongation may be
a consequence of an unfavorable balance between sympathetic and parasympathetic activities. Sympathetic
predominance accompanied by dispersion of repolariza-

tion reected in QTc prolongation may result in ventricular electrical instability and increase the risk of fatal
myocardial infarction. It can thus be speculated that
changes in autonomic nervous system (ANS) activity,
particularly the sympatho-vagal balance contributes to
the prolongation of QTc. We have therefore conducted
a series of studies to develop computer algorithms to
measure cardiac depolarizationrepolarization times
and to accomplish the analysis of ECG RR interval
power spectral analysis simultaneously by using the
CM5 lead ECG [70]. Additionally, we have applied

Fig. 5. Electrocardiographic determination of cardiac depolarization/repolarization process.

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these techniques to assess diabetic patients with dierent

degrees of neuropathy in terms of cardiac autonomic
functions and myocardial depolarizationrepolarization
processes [34,35,70]. Ten patients with ischemic heart
disease (IHD), 30 patients with diabetes mellitus, and
10 control subjects (CON) volunteered for these studies.
The patients with diabetes mellitus were further divided
into three subgroups according to the severity of neuropathy: patients without any neuropathy (N0), with
peripheral neuropathy (N1), and with autonomic neuropathy (N2). Computer-aided cardiac depolarization
repolarization analyses were performed to assess ECG
activation time (AT), ARI, and RT.
Figs. 6 and 7 represent a typical set of computeraided ECG analysis results obtained from a healthy
individual and a patient with ischemic heart disease,
respectively. Note the remarkable dierences in heart
rate variability and RT representing the time required
for completing cardiac repolarization. ECG R-wave
trigger-averaged signals were displayed on the right corner of the gures from which the time of maximal dV/dt
of the T waves was determined.
Results shown in Fig. 8 indicated that there were signicant increases (prolongation) in RT in N1, N2, and
IHD as compared with CON and N0. Thus, our newly
implemented computer system could be used for examining the cardiac depolarizationrepolarization process
in order to study patients with ischemic heart disease
and with varying degrees of diabetic autonomic
neuropathy.
The hypothesis of adrenergic imbalance as the cause
of a long QT interval has been supported by experimen-

245

tal work demonstrating prolongation of the QT interval

after either right satellite ganglion ablation or left satellite ganglion stimulation. Schwartz et al. [61,62] suggested that regional sympathetic imbalance involving
only a portion of the sympathetic supply might result
in long QT syndrome. It is reasonable to conclude that
the sympathetic imbalance may have caused the QT
interval and RTc prolongation which increased risk
for malignant arrhythmias and thereby be responsible
for cardiac sudden death. Conversely, increased vagal
activity or decreased sympathetic activity decreases vulnerability to ventricular brillation or repetitive ventricular response in ischemic animals. Thus, on the basis of
many previous studies, autonomic dysfunction is associated with the high-risk patients susceptibility to ventricular arrhythmias, resulting in sudden death.
2.2. Cardiac autonomic activity assessment
Glowniak et al. [15] did one of the rst studies relating heart rate variability to death in cardiac patients. In
this study the variance of RR interval length in short
segments of ECG recordings (30 RR intervals) was calculated. In later studies, 24-h ECG recordings were used
to obtain a measure of overall heart rate variability.
These studies have also provided that myocardial infarction lowers beat-to-beat heart rate (HR) variability and
that diminished heart rate variability is associated with
an increased risk for ventricular brillation and sudden
cardiac death [61,62,70] (also see Figs. 6 and 7). Decreased vagal tone diminishes HR variability and predisposes ventricular brillation in animals with

Fig. 6. A typical set of computer out put from a healthy individual showing the raw ECG, RR interval and trigger-averaged signals for determining
cardiac depolarization/repolarization characteristics, i.e., activation recovery interval (ARI), cardiac recovery time (RT), and QT interval,
respectively.

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Fig. 7. A typical set of computer out put from a patient with ischemic heart disease showing the raw ECG, RR interval and trigger-averaged signals
for determining cardiac depolarization/repolarization characteristics.

Fig. 8. Group data on myocardial depolarization/repolarization period. Control (CON), diabetic patients without any neuropathy (N0), with
peripheral neuropathy (N1) and with autonomic neuropathy (N2) and ischemic heart disease (IHD).

experimental myocardial ischemia. Many studies have

demonstrated that increased sympathetic activity during
experimental ischemia or infarction promotes ventricular brillation [10,11].
Fig. 9 represents our method for cardiac autonomic
activity assessment by means of electrocardiogram
(ECG) RR interval power spectral analysis [34,35,70].
The ECG RR interval, or inter-beat interval of heart
rate is determined by the net eect of sympathetic and
parasympathetic input. The heart rate variability
(HRV) power spectral analysis has been proven as a reli-

able non-invasive method and has provided a comprehensive quantitative and qualitative evaluation of
neuroautonomic function under various physiological
conditions [1,2,34,35,48,53,70]. In general, the high-frequencies (>0.15 Hz) of HRV are associated with almost
entirely vagal nerve activity and low-frequencies (<0.15
Hz) of HRV might be mediated by both vagal and
SNS activities [1,53].
We have examined the possible sympatho-vagal functional dierences at rest and during progressive exercise
to exhaustion among diabetic patients, normal controls

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247

Fig. 9. A schematic representation of our ECG RR interval power spectral analysis for evaluation of cardiac autonomic activity.

and endurance athletes by means of our computerimplemented ECG RR power spectral analysis. Since
heart rate power between 0.04 and 0.15 Hz was most
sensitive and specic in dierentiating patients and controls [59], we analyzed low frequency (0.030.15 Hz, LO)
and high vagal component (0.150.4 Hz, HI) by integrating the spectrum for the respective bandwidth. In
addition, sympathetic nervous system activity (SNS)
and parasympathetic nervous system activity (PNS)
indices were calculated as the ratio of LO/HI and HI/
TOTAL, respectively.

Fig. 10 shows represents typical sets of raw RR

interval and the corresponding amplitude spectral data
obtained from a non-insulin dependent diabetes
(NIDDM) patient and a non-diabetic healthy individual
(CONT), respectively, during quiet resting. Note that
mean heart rate was subtracted from the original RR
interval data, thus only the RR variability could be directly compared in this gure. It can be readily seen that
RR variability in NIDDM was markedly reduced as
compared with the CONT. The corresponding RR
interval spectra also show vast dierences in both LO

Fig. 10. A typical set of ECG RR interval power spectra obtained from a patient with non-insulin dependent diabetes and from a healthy
individual.

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T. Moritani et al. / Journal of Electromyography and Kinesiology 15 (2005) 240255

and HI frequency components between these subjects.

The most striking feature of the spectra is the contrasting HI vagal component between NIDDM and CONT.
These data suggest that a considerable reduction of
overall cardiac autonomic nervous system and the withdrawal of the vagal activity might be present in the patients with NIDDM.
Group data indicated that there were signicant differences in the HI vagal frequency components among
three groups (NIDDM < CONT < ENDR, p < 0.01),
PNS index (NIDDM < CONT < ENDR, p < 0.01) and
SNS index (NIDDM > CONT > ENDR, p < 0.01),
respectively. In the context, the simultaneous assessment
of the extent of cardiac parasympathetic nervous activities and imbalance of sympatho-vagal nervous activities
found in our studies [34,35,70] may provide the important information of prognosis in the patients vulnerability for ventricular arrhythmias. In the clinical setting,
where coexisting IHD and diabetes mellitus is common,
attention must be paid in managing such patients and
the assessment of autonomic nervous function.

continuously by our computer-aided ECG RR interval

power spectral analysis and ECG Q-T interval measurements, respectively. Results indicated that upon cigarette smoking there were signicant increases in heart
rate and cardiac sympathetic nervous activity together
with a signicant reduction in the parasympathetic
activity. Oral sesamin administration showed a marked
suppressive eect upon these changes. Placebo trial also
showed a signicant prolongation (389 11 to 405 13
ms, p < 0.01) in ECG Q-T interval immediately after
smoking, which has been known as one of the major risk
factors for sudden cardiac death, while sesamin intake
prevented such an increase in QT interval (383 4 to
398 4 ms, p > 0.05). These data strongly suggest that
sesamin can be a useful supplement for reducing the adverse eects of smoking upon cardiac autonomic nervous system. Our subsequent animal experiments
clearly indicated that sesamin may enhance lipid peroxidation (LPO) degradation in the liver resulting in the
strong protective eects against exercise-induced plasma
lipid peroxidation [23].

2.3. Changes in cardiac autonomic activities during

smoking and the eects of antioxidant

3. Etiology of obesity and autonomic nervous system

Sesame seeds have been regarded as a high nutritional

value food to promote good health and prevention of
aging. Sesamin is one of the lignans existing exclusively
in sesame oil. It has recently been demonstrated that sesamin is rst transported to the liver where it is metabolized to an antioxidative form, catechol sesamin [46]. We
therefore determined the eects of this new antioxidant
substance sesamin during acute smoking on cardiac
depolarization/repolarization characteristics and cardiac
autonomic nervous activities. Nine male college students
were tested during acute cigarette smoking after oral
administration of placebo or sesamin capsules given at
random. Cardiac sympatho-vagal activities and cardiac
depolarization/repolarization processes were evaluated

Obesity, a common and important health hazard, is

associated with an increased incidence of hypertension,
congestive heart failure, diabetes, and cardiac sudden
death, as well as an overall increase in mortality rate
[54,55]. The causes of most cases of human obesity are
still unknown. Recent identication of obese genes (leptin, uncoupling protein (UCP) families and Trp64Arg
polymorphism of the b3-adrenergic receptor) has increased our understanding of the patho-physiology of
obesity and related diseases [14,28,57,58,72]. Fig. 11
schematically summarizes current hypothesis explaining
the major role of autonomic nervous system activity and
its principal components for regulating our body weight.
3.1. Role of autonomic nervous system in body weight
regulation

Role of ANS in Body Weight Regulation

Hypothalamus

Leptin

VMH

LH

Satiety Ctr
(SNS)

Appetite Ctr
(PNS)

Food
Intake

Sympathetic
3AR
White adipose
tissue

Fat
Mobilization

3AR
Brown adipose
tissue UCP1

Energy
Expenditure

Fig. 11. A block diagram showing a current hypothesis of body weight

regulation and fat metabolism.

Bray [8] has proposed the MONA LISA hypothesis,

an acronym for Most Obesities kNown Are Low In
Sympathetic Activity indicating that obesity is associated with a relative or absolute reduction in the activity
of the thermogenic component of the sympathetic nervous system.
Since the b3-adrenergic receptor plays a signicant
role in the control of lipolysis and thermogenesis in
brown adipose tissue through autonomic nervous system (ANS) activity (please see Fig. 11), we rst determined the prevalence of the polymorphism in 204
subjects [65,66,69]. Results indicated that the subjects
with the variant, even the heterozygotes, demonstrated
signicantly lower resting ANS activity than normal

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249

Fig. 12. Autonomic activity among subjects with variant b3-adrenergic receptor genes.

subjects, whereas the clinical characteristics did not differ between groups (see Fig. 12).
Autonomic responsiveness was then assessed in age
and height-matched 27 obese and non-obese women
during resting and acute cold exposure (10 C for 15
min) in an environmental chamber [29]. Prior to this
experiment, 6 subjects were studied during pharmacological blockade experiments (parasympathetic muscarinic blocker, atropine and b-sympathetic blocker,
propranolol) to examine the eects of autonomic blockade on energy metabolism.
Results indicated that the complete abolishment of
the autonomic nervous activity signicantly decreased
resting metabolic cost amounting to approximately

310 kcal/day, strongly suggesting that ANS does play
a signicant role in resting metabolism [29]. Plasma leptin was signicantly higher in the obese as compared
with non-obese group (p < 0.001) [30]. There was a
highly signicant correlation (r = 892, p < 0.001) between leptin concentration and % body fat [31]. The
sympathetic nervous system activity index (SNS) to leptin ratio (sympathetic responsiveness to leptin) was also
found to be signicantly smaller (p < 0.001) in obese as
compared to non-obese group [30].
Capsaicin is the major pungent principle in various
species of Capsicum fruits such as hot chili pepper. It
has been shown that dietary supplementation of capsaicin in high fat diets lowered the adipose tissue weight
and serum triglyceride concentration in rats due to

enhancement of energy metabolism. Our subsequent

studies [29,3133,42,44,45] involving adults and children
have demonstrated that upon the acute cold exposure,
capsaicin-containing food intake or high fat diets, the
obese group demonstrated signicantly lower spectral
power component associated with thermogenesis as well
as signicantly lower responsiveness (see Fig. 13).
Our data strongly support the MONA LISA hypothesis and further suggest that obese individuals may show
much lower autonomic responsiveness against thermogenic perturbations such as acute cold exposure and
diet-induced thermogenesis. Signicantly lower sympathetic activities per leptin also dictate that obese women
might have a reduced or impaired autonomic responsiveness associated with thermogenic component of the
sympathetic nervous system and/or leptin resistance.
Our data indicate that regardless of the resting level of
sympatho-vagal activities, the reduced sympathetic
responsiveness to thermogenic perturbation, which
may cause impaired diet-induced thermogenesis and further weight gain, could be an important etiological factor leading to obesity.
3.2. Exercise training and autonomic nervous system
Our previous data suggest that obese children, as well
as adults, possess both reduced sympathetic and parasympathetic nervous activities as compared to lean individuals [2,45,71]. Such autonomic reductions associated

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Fig. 13. Comparison of autonomic responsiveness between normal and obese individuals during cold exposure. Note the marked dierence in the
response of VLO component associated with sympathetic thermogenesis.

with the amount of body fat in an inactive state, might

be an etiological factor of the onset or development of
obesity. On the other hand, although exercise training
not only decreases abdominal visceral fat, but also improves general health, it is recommended for obese people with no contraindications. However, the reduced
ANS activity frequently observed in these obese individuals thereby makes them much more prone to develop
exercise complications, including malignant arrhythmias, and so exercise prescription should be carefully
designed.
We have recently developed a new exercise prescription method based upon cardiac parasympathetic activity [63,64]. To further verify the validity of this new
method, we examined the acute eects of aerobic exercise upon sympatho-vagal activities, b-endorphin, atrial
and brain natriuretic peptides (ANP and BNP), and
EEG. Measurements consisted of beat-by-beat systolic
and diastolic blood pressures (SBP and DBP) and cardiac sympatho-vagal activities by means of ECG RR
interval power spectral analysis. Results suggested that
moderate exercise could bring about post-exercise hypotension by modulating natriuretic peptides and b-endorphin levels with subsequent changes in autonomic
nervous system and brain EEG a-wave activities [36].
We also investigated the eects of long-term physical
training on ANS in 305 school children (20 min/day, 5
times/wk for 12 month) [43] and 18 obese middle-aged
individuals (30 min/day, 3 times/wk, for 12 wks) [2]. Results indicated that long-term exercise, even for 20 min a
day with mild intensity, could signicantly improve both
the sympathetic and vagal nervous system activities of

the children with initially lower HRV. Similarly, the

exercise training resulted in a signicant decrease in
body mass, BMI, and % fat together with a signicant
increase in the aerobic working capacity (anerobic
threshold). Total cholesterol, LDL-C, and leptin were
also signicantly decreased after exercise training. Our
power spectral data indicated that the sympatho-vagal
frequency component and total power were signicantly
increased after training, suggesting a strong possibility
of enhanced ANS activities with regularly performed
exercise training, particularly the parasympathetic activity, even in the middle-aged individuals.

4. Functional electrical stimulation for health and disease

4.1. Electrical stimulation vs. voluntary contraction
Electrical stimulation (ES) produces skeletal muscle
contractions as a result of the percutaneous stimulation
of the peripheral nerve. Clinically, the use of ES has
been shown to potentially improve or compensate for
disadvantages in disabled or chronic patients with physical inactivity. In fact, ES of skeletal muscles might not
only improve cardiovascular function for tetra or paraplegics, but may also increase the strength and endurance of their paralyzed muscles during daily activity
such as wheelchair locomotion or body transfer
[12,24]. In addition, previous animal experiments have
shown that glucose transport activity is considerably
higher in Type II than Type I bers when ES is employed [25,56].

T. Moritani et al. / Journal of Electromyography and Kinesiology 15 (2005) 240255

Unlike the orderly recruitment of motor units (MUs)

during low intensity voluntary exercise in which Type I
slow-twitch bers are utilized rst [16,39,40], during ES,
large and fatigable fast-twitch motor units (MUs) with
glycolytic bers are activated rst. Because of their larger axons, which in turn have much lower electrical
resistance for a given externally applied electrical current [9,20,68], large fast-twitch MUs would be activated
before slow-twitch MUs, suggesting reversed size principle of MUs recruitment by ES. Our most recent study
[20] has clearly demonstrated that fast MUs are selectively activated during ES.
The selective activation of fast MUs by ES would be
quite useful in preventing and treating patients with diabetes and chronic diseases with subsequent muscle atrophy leading to bed-ridden conditions. ES has been
traditionally employed for muscle strengthening, maintenance of muscle mass and strength, and restoring muscular functions following stroke or spinal cord injury.
Exercise increases glucose uptake by the translocation
of GLUT-4 glucose transporters, similar to the action
of insulin, but though independent mechanisms
[17,22]. It is quite reasonable to assume that ES may become a better approach to enhance the glucose transport
activity in skeletal muscle. This low intensity ES without
requiring vigorous voluntary exercise ensures the activation of Type II bers with subsequent enhancement of
post-stimulation glucose uptake, particularly for those
individuals who are unable to exercise due to orthopedic
problems or other complications.
We have therefore performed a series of experiments
[18,19] to establish the most optimal ES frequency,
intensity, duration, and pattern and to directly measure
oxygen consumption and whole body glucose uptake
by means of glucose disposal rate (GDR) in hyperinsulinemiceuglycemic clamp, respectively. In the rst
experiment, eorts were made to determine the optimal
stimulation frequency that would induce the highest
oxygen uptake during a 20-min sustained ES to the
right quadriceps muscle. The polarity (monophasic vs.
biphasic) and stimulation-rest duty cycle were also
examined. In addition, the knee extension force measurement was simultaneously made during these various patterns of muscle surface stimulations. It was
found that either lower or higher than 20 Hz stimulation frequency with 1 s on 1 s o duty cycle resulted
in much lower oxygen consumption and the total
amount of accumulated force. In fact stimulation at
60 Hz with identical ES pattern showed marked force
loss towards the end of ES due to impaired neuromuscular transmission or membrane excitation, i.e., high
frequency fatigue [13,37,38]. We therefore adopted the
stimulation pattern with 20 Hz frequency and 1 s on
o duty cycle with biphasic polarity as the optimal conditions for ES and used this protocol in the subsequent
invasive study.

251

For the subsequent experiment, 8 male college students volunteered for the invasive hyperinsulinemic
euglycemic clamp measurement. The subject was in
the supine position with both knees extended and surface electrodes were placed over the motor points in
the proximal and middle portion of the thigh. Both
quadriceps muscles were then simultaneously stimulated to induce isometric muscle contractions for a period of 20 min. Stimulation consisted of square-wave
biphasic pulses of 0.2 ms duration at 20 Hz. Stimulator
output was limited to 80 volts for painless muscle contraction. Oxygen consumption determined by respiratory gas exchange analysis was rapidly increased by
approximately 2-fold in response to muscle stimulations (3.2 0.1 to 5.7 0.1 ml/kg/min (means SE),
p < 0.05). The increase in oxygen consumption was
maintained throughout the stimulation period, and
then returned to the baseline level immediately after
the cessation of the stimulation. Similarly, whole body
glucose uptake determined by glucose disposal rate
(GDR) in hyperinsulinemiceuglycemic clamp was
acutely increased in response to electrically-induced
contractions from 7.2 0.4 mg/kg/min to 9.7 0.9
mg/kg/min (p < 0.01). Furthermore, GDR remained
elevated during the post-stimulation period for at least
90 min (030 min, 10.1 0.6; 3060 min, 10.0 0.4;
6090 min, 11.4 0.8 mg/kg/min, p < 0.01 vs. baseline)
while the steady-steady insulin concentration during
clamp was within the physiological range for all the
subjects and also sucient to suppress endogenous glucose production (70 U/ml). These results strongly
suggested that, similar to voluntary exercise, involuntary muscle contraction leads to substantial enhancement of energy and glucose utilization in humans (see
Figs. 14 and 15).
In the second experiment we further examined the
acute metabolic eects of ES to lower extremities in
comparison with voluntary cycle exercise (VE) at an
identical intensity. In eight male subjects, lying in the supine position, both lower leg (tibialis anterior and triceps surae) and thigh (quadriceps and hamstrings)
muscles were sequentially stimulated to co-contract in
an isometric manner at 20 Hz with a 1-s ono duty cycle for 20 min. Despite of the small elevation of oxygen
uptake by 7.3 0.3 ml/kg/min during ES, the blood lactate concentration was signicantly increased by
3.2 0.3 mmol/l in initial period (5 min) after the onset
of the ES (p < 0.01), whereas VE showed no such
changes at an identical oxygen uptake (7.5 0.3 ml/kg/
min). ES also induced enhanced whole body carbohydrate oxidation as shown by the signicantly higher
respiratory gas exchange ratio than VE (p < 0.01). These
data indicated increased anerobic glycolysis by ES. Furthermore, whole-body glucose uptake determined by
GDR during euglycemic clamp demonstrated a signicant increase during and after the cessation of ES for

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T. Moritani et al. / Journal of Electromyography and Kinesiology 15 (2005) 240255

Fig. 14. Pictures showing experimental setup for performing electrical stimulation and voluntary exercise at identical energy consumption.

Fig. 15. Time course of changes in whole body glucose uptake during electrical stimulation and voluntary exercise.

at least 90 min (p < 0.01). This post ES eect was significantly greater than that of the post VE period
(p < 0.01). These results suggested that ES can substantially enhance energy consumption, carbohydrate oxidation, and whole body glucose uptake at low intensity of
exercise. We therefore concluded that ES may become a
useful modality that could enhance, through the insulinindependent mechanisms, glucose uptake in skeletal
muscle of those patients with peripheral insulin resistance, such as non-insulin-dependent diabetes mellitus
and/or chronic patients with progressive muscle
atrophy.

Acknowledgments
This work was supported in part by a Grant-in-Aid
for Scientic Research (B) No. 15300231 from Japan
Society for the Promotion of Science. We also thank
Mr. Aaron M. Saikin for his careful reading of the
manuscript.
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T. Moritani et al. / Journal of Electromyography and Kinesiology 15 (2005) 240255

Toshio Moritani was born in Japan in
1950. He received his Ph.D. degree in
Sports Medicine from the University of
Southern California in 1980 under the
direction of Dr. Herbert A. deVries. In
1985, following faculty appointments at
the University of Texas at Arlington and
Texas A&M University, he returned to
Japan and joined the Department of
Integrated Human Studies at Kyoto
University. In 1992, he was appointed
Associate Professor of Applied Physiology at the Graduate School of Human and Environmental Studies
at Kyoto University and became Professor since 2000. He is
currently Director of the Laboratory of Applied Physiology. Dr.
Moritani has been elected as Fellow of the American College of
Sports Medicine. Dr. Moritani is the Editor of the Journal of
Electromyography and Kinesiology. He is also serving as a member
of the Editorial Board for the European Journal of Applied
Physiology and Editorial Consultant for the Journal of Biomechanics. He has also served as one of the Council Members and
currently being the President Elect of the International Society of
Electrophysiology and Kinesiology.
Tetsuya Kimura received his M.Sc. degree
in Human and Environmental Studies from
Kyoto University in 2004. He is currently
working for the Ph.D. degree under the
direction of Dr. Toshio Moritani. His current research interest includes the activation
strategies of motor units during exhaustive
muscle contraction, associated with changes both in their mechanical function and
metabolic state.

255

Taku Hamada obtained M.Sc. degree from

Nippon Sports Science University (Tokyo,
Japan) in 1995. Then, he joined the Human
Performance Laboratory, Department of
Kinesiology,
McMaster
University
(Ontario, Canada). He worked on interaction of evoked twitch contractile properties,
muscle fatigue, and ber types in the laboratory as research student under the
supervision of Dr. Digby Sale from 1995 to
1998. He received his Ph.D. degree from
Kyoto University (Kyoto, Japan) under the
direction of Drs. Toshio Moritani and Tatsuya Hayashi in 2004. His
research interests are neuromuscular and metabolic physiology. His
current research has focused on regulation of muscle glucose metabolism and insulin sensitivity with reference to exercise and diabetes.
This work has conducted on humans and animal models with various
electrophysiological and biochemical techniques.
Narumi Nagai is a Registered Dietitian and
the Director of the Laboratory of Human
Nutrition at Okayama Prefectural University. Following the graduation of the
Department of Food Science at Japan
Womens University in 1999, she worked in
the Laboratory of Applied Physiology of
the Graduate School of Human and Environmental Studies, Kyoto University under
the direction of Dr. Moritani and received
Ph.D. degree in 2004. In 2003, she was
appointed as Lecturer of the Department of
Nutritional Science at Okayama Prefectural University, where she is
currently investigating the role of autonomic nervous system and
nutritional as well as genetic factors on the cause of obesity with
younger generation.